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https://hdl.handle.net/2144/31236

Abstract

Periodontitis (PD) and type II diabetes mellitus (T2D) are chronic inflammatory diseases that affect populations worldwide. While it has been well established clinically that T2D is a risk factor for PD, previous studies have failed to determine the molecular mechanism linking T2D and PD. As a result, the objectives of this study were as follows: to characterize the inflammation present in gingival tissue immune cells in subjects with periodontitis (PD) and subjects with type II diabetes mellitus and periodontitis (T2D/PD) compared with healthy subjects (H); to identify the effect of T2D on inflammation in PD; and to determine the predominant cell type responsible for the production of pro-inflammatory cytokines. Using flow cytometry to sort and purify cells based on CD45+ cell surface expression into CD4+, CD8+, CD11b+, CD19+, and CD56+ cell subgroups, we used the Enzyme Linked ImmunoSpot (ELISPOT) assay to quantify cytokine production in gingival cells from the three groups (H, PD, and T2D/PD). We identified CD4+ T helper cells as the predominant cell type in gingival tissues from T2D/PD subjects and found that these cells produced higher concentrations of Th1 cytokines IL-2, IL-10, IFN-y, and TNF-a in T2D/PD subjects than in H and PD subjects. As a result, we concluded that T2D increases inflammation in PD by an increase Th1 cell persistence.